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I read the paper by Fletcher and colleagues with interest. (Gut 2004;53:168–73.)
In their earlier study,1 the group reported the existence of an unbuffered acid pocket in 60% of study subjects which extended for approximately 2 cm (median length) in the postprandial period. Furthermore, when pre and postprandial pH step up distances were measured and correlated with clips fixed to the oesophagus, this acid pocket was localised to a region “just above” the squamocolumnar junction. It would be fair to infer then, that if a pH sensor was firmly implanted just above the squamocolumnar junction, it would record a prolonged acid reflux event in the postprandial state as the probe would be continuously bathed in acid from this reservoir. This is distinct from intermittent acid reflux events due to transient lower oesophageal sphincter relaxations or straining.
In their more recent paper,2 greater acid exposure at the squamocolumnar junction was found compared with a site located 5 cm proximally (standardised recording point), which intuitively is not unexpected. This is especially so if DeMeesters hypothesis (which was alluded to in the manuscript) were to be accepted which proposes that the lower oesophageal sphincter, incorporating the squamocolumnar junction, opens up and becomes part of the stomach in the postprandial period. However, the authors have stated that there was no significant difference in the mean length of acid reflux episodes when both sites were compared. This appears to be at odds with the first study as one would have expected to observe a prolonged acid reflux event at the distal oesophageal recording site (that is, just above the squamocolumnar junction). However, this was not the case. In addition, presentation of data in the results section of the current study show a distinct lack of emphasis regarding the “acid pocket theory” which would lead one to assume that this was not observed. How do the authors reconcile these observations from their two studies?
We thank Dr Nandurkar for his interest in our recent papers regarding luminal acidity at the gastro-oesophageal junction following meals.
In our first study, we observed a postprandial region of high acidity in the cardia region and extending across the Z-line.1 The presence of this postprandial acid pocket at the cardia has been confirmed by two other groups2,3
In our more recent study (Gut 2004;53:168–73), we observed a high degree of acid exposure when a pH electrode was clipped to the squamous mucosa which is proximal to the Z-line.
Dr Nandurkar wondered why we did not observe more prolonged acid exposure in the second study if the postprandial acid pocket extends into the distal oesophagus. There are several reasons for the apparent differences in the two studies. The first is that the design and methodology of the two studies were different. The first study involved slowly withdrawing a pH probe at 1 cm increments every minute from the distal stomach into the oesophagus and was performed after a large fatty meal with the patient in a semirecumbent position. In contrast, the second study employed a static probe fixed to the distal oesophagus and which recorded both fasting and postprandial pH over a 24 hour ambulatory period. The difference in duration of the recording of pH in the distal oesophagus between the two studies and the differences in the relationship to food intake and in posture and mobility make it difficult to directly compare the two studies. In our second study, we did observe that the acid exposure of the most distal oesophagus was more during the postprandial period, consistent with the observations of the first study. However, we acknowledge that the duration of acid exposure of the most distal oesophagus during the postprandial period with the fixed probe was not as great as that observed in our earlier study when the probe was slowly withdrawn from the stomach into the oesophagus.
It is possible that the methodology employed in the first study could exaggerate the degree of proximal extension of the unbuffered acid pocket into the distal oesophagus. This might be due to the pH probe carrying over some acidic juice from the cardia acid pocket into the oesophagus and this taking time to be fully cleared/neutralised. It is always difficult to know the extent to which the technique used to measure physiology may be altering events.
What is clear from both of our studies and the two other groups which have undertaken similar studies is that during the postprandial period, (a) there is a region of relatively unbuffered high acidity in the proximal cardia region of the stomach and (b) this acid frequently encroaches on the distal oesophageal mucosa.1–3
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